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乳腺肿瘤富含高活性的低分子量细胞周期蛋白E,并导致细胞周期蛋白依赖性激酶2功能失调,但其低分子量片断的形成机制尚不清楚。对乳腺肿瘤低分子量细胞周期蛋白E通过翻译后水平的某种蛋白酶作用形成的这一假说进行了探讨。钙离子可诱发乳腺肿瘤培养细胞ZR75周期蛋白E剪切为分子量与乳腺肿瘤组织相似的小分子片断。纯化Calpeptin能抑制上述过程,提示剪切过程与钙离子依赖性蛋白酶(Calpain)活性有关。同样,钙离子+纯化Calpain也能引起乳腺肿瘤细胞和组织免疫沉淀周期蛋白E的剪切。钙离子还能引起肿瘤细胞和组织Calpain调节(小)亚基有限水解,表明Cal-
Breast neoplasms are rich in high-activity low-molecular-weight cyclin E and result in dysfunctional cyclin-dependent kinase 2, but the mechanism by which low molecular weight fragments are formed remains unclear. The hypothesis that breast cancer low-molecular-weight cyclin E is formed by a protease action at the post-translational level is explored. Calcium ions can induce breast tumor cells cultured ZR75 cycle protein E cut into molecular weight and breast tumor tissue similar to the small molecule fragments. Purified Calpeptin can inhibit the above process, suggesting that the shearing process and calcium-dependent protease (Calpain) activity. Similarly, calcium + purified Calpain also causes the cleavage of cyclin E by the immunoprecipitates of breast tumor cells and tissues. Calcium ions also caused limited hydrolysis of the (small) subunit of Calpain regulated by tumor cells and tissues, indicating that Cal-